Telomeres are the structures capping the ends of chromosomes, and are critical to the maintenance of chromosomal integrity and replication potential. Telomere length is lost during each cycle of proliferation, and reduction below a critical minimum length results in cell death (Lingner, J., et al. (1995) Science 269:1533–1534). The enzyme telomerase is capable of restoring telomere length, and is nearly universally present in tumor cells, while usually absent in normal cells (Hiyama, E., et al. (1996) J. Natl. Cancer Inst., 88:116–122). The critical nature of its function, and its selective presence in tumor cells, suggest it is a desirable target for cancer chemotherapy. Unfortunately, however, telomerase inhibitors do not appear to have significant antitumor activity, probably because telomere shortening occurs slowly, thereby allowing more cycles of undesired cell proliferation. In addition, current techniques for measuring changes in telomerase activity and telomere biology are of limited sensitivity.
Accordingly, a need exists for developing more efficacious cancer therapies, including combination drug therapies, that specifically target cellular events associated with the cancer phenotype. In addition, improved techniques for measuring cellular changes associated with the cancer phenotype, e.g., telomere biology, are needed.